Host control of malaria infections: constraints on immune and erythropoeitic response kinetics.

The two main agents of human malaria, Plasmodium vivax and Plasmodium falciparum, can induce severe anemia and provoke strong, complex immune reactions. Which dynamical behaviors of host immune and erythropoietic responses would foster control of infection, and which would lead to runaway parasitemi...

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Autores principales:	Philip G McQueen, F Ellis McKenzie
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2008
Materias:	Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/3b6a69e18b2f4370b521a196a3c586c9
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spelling	oai:doaj.org-article:3b6a69e18b2f4370b521a196a3c586c92021-11-25T05:42:02ZHost control of malaria infections: constraints on immune and erythropoeitic response kinetics.1553-734X1553-735810.1371/journal.pcbi.1000149https://doaj.org/article/3b6a69e18b2f4370b521a196a3c586c92008-08-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/18725923/?tool=EBIhttps://doaj.org/toc/1553-734Xhttps://doaj.org/toc/1553-7358The two main agents of human malaria, Plasmodium vivax and Plasmodium falciparum, can induce severe anemia and provoke strong, complex immune reactions. Which dynamical behaviors of host immune and erythropoietic responses would foster control of infection, and which would lead to runaway parasitemia and/or severe anemia? To answer these questions, we developed differential equation models of interacting parasite and red blood cell (RBC) populations modulated by host immune and erythropoietic responses. The model immune responses incorporate both a rapidly responding innate component and a slower-responding, long-term antibody component, with several parasite developmental stages considered as targets for each type of immune response. We found that simulated infections with the highest parasitemia tended to be those with ineffective innate immunity even if antibodies were present. We also compared infections with dyserythropoiesis (reduced RBC production during infection) to those with compensatory erythropoiesis (boosted RBC production) or a fixed basal RBC production rate. Dyserythropoiesis tended to reduce parasitemia slightly but at a cost to the host of aggravating anemia. On the other hand, compensatory erythropoiesis tended to reduce the severity of anemia but with enhanced parasitemia if the innate response was ineffective. For both parasite species, sharp transitions between the schizont and the merozoite stages of development (i.e., with standard deviation in intra-RBC development time <or=2.4 h) were associated with lower parasitemia and less severe anemia. Thus tight synchronization in asexual parasite development might help control parasitemia. Finally, our simulations suggest that P. vivax can induce severe anemia as readily as P. falciparum for the same type of immune response, though P. vivax attacks a much smaller subset of RBCs. Since most P. vivax infections are nonlethal (if debilitating) clinically, this suggests that P. falciparum adaptations for countering or evading immune responses are more effective than those of P. vivax.Philip G McQueenF Ellis McKenziePublic Library of Science (PLoS)articleBiology (General)QH301-705.5ENPLoS Computational Biology, Vol 4, Iss 8, p e1000149 (2008)
institution	DOAJ
collection	DOAJ
language	EN
topic	Biology (General) QH301-705.5
spellingShingle	Biology (General) QH301-705.5 Philip G McQueen F Ellis McKenzie Host control of malaria infections: constraints on immune and erythropoeitic response kinetics.
description	The two main agents of human malaria, Plasmodium vivax and Plasmodium falciparum, can induce severe anemia and provoke strong, complex immune reactions. Which dynamical behaviors of host immune and erythropoietic responses would foster control of infection, and which would lead to runaway parasitemia and/or severe anemia? To answer these questions, we developed differential equation models of interacting parasite and red blood cell (RBC) populations modulated by host immune and erythropoietic responses. The model immune responses incorporate both a rapidly responding innate component and a slower-responding, long-term antibody component, with several parasite developmental stages considered as targets for each type of immune response. We found that simulated infections with the highest parasitemia tended to be those with ineffective innate immunity even if antibodies were present. We also compared infections with dyserythropoiesis (reduced RBC production during infection) to those with compensatory erythropoiesis (boosted RBC production) or a fixed basal RBC production rate. Dyserythropoiesis tended to reduce parasitemia slightly but at a cost to the host of aggravating anemia. On the other hand, compensatory erythropoiesis tended to reduce the severity of anemia but with enhanced parasitemia if the innate response was ineffective. For both parasite species, sharp transitions between the schizont and the merozoite stages of development (i.e., with standard deviation in intra-RBC development time <or=2.4 h) were associated with lower parasitemia and less severe anemia. Thus tight synchronization in asexual parasite development might help control parasitemia. Finally, our simulations suggest that P. vivax can induce severe anemia as readily as P. falciparum for the same type of immune response, though P. vivax attacks a much smaller subset of RBCs. Since most P. vivax infections are nonlethal (if debilitating) clinically, this suggests that P. falciparum adaptations for countering or evading immune responses are more effective than those of P. vivax.
format	article
author	Philip G McQueen F Ellis McKenzie
author_facet	Philip G McQueen F Ellis McKenzie
author_sort	Philip G McQueen
title	Host control of malaria infections: constraints on immune and erythropoeitic response kinetics.
title_short	Host control of malaria infections: constraints on immune and erythropoeitic response kinetics.
title_full	Host control of malaria infections: constraints on immune and erythropoeitic response kinetics.
title_fullStr	Host control of malaria infections: constraints on immune and erythropoeitic response kinetics.
title_full_unstemmed	Host control of malaria infections: constraints on immune and erythropoeitic response kinetics.
title_sort	host control of malaria infections: constraints on immune and erythropoeitic response kinetics.
publisher	Public Library of Science (PLoS)
publishDate	2008
url	https://doaj.org/article/3b6a69e18b2f4370b521a196a3c586c9
work_keys_str_mv	AT philipgmcqueen hostcontrolofmalariainfectionsconstraintsonimmuneanderythropoeiticresponsekinetics AT fellismckenzie hostcontrolofmalariainfectionsconstraintsonimmuneanderythropoeiticresponsekinetics
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Host control of malaria infections: constraints on immune and erythropoeitic response kinetics.

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